Cranial neuropathy

DIES-associated neuropathy has a variety of chnical presentations, including painful symmetric or asymmetric sensorimotor neuropathy, distal sensory neuropathy, mononeuritis multiplex, and demyelinating polyneuropathy (Gherardi et al. 1998). Cranial neuropathy without evidence of a more generahzed neuropathy may occur, typically as a facial nerve palsy in association with parotidomegaly (Itescu et al. 1990 Brew 2003). The neuropathy develops subacutely over days to weeks. In some cases, muscle weakness may be a result of an inflammatory myositis (Kazi et al. 1996). 

Cavanagh JB, Buxton PH. 1989. Trichloroethylene cranial neuropathy Is it really a toxic neuropathy or does it activate latent herpes virus J Neurol Neurosurg Psychiatry 52 297-303. 

Nonpulmonary manifestations are extremely common and include nausea, vomiting, diarrhea, myalgias, arthralgias, polyarticular arthritis, skin rashes, myocarditis and pericarditis, hemolytic anemia, meningoencephalitis, cranial neuropathies, and ft n i I lain - Bar re syndrome. Systemic symptoms generally clear in 1 to 2 weeks, whereas respiratory symptoms may persist up to 4 weeks. 

Botulism. Clinical features include symmetric cranial neuropathies (i.e., drooping eyelids, weakened jaw clench, and difficulty swallowing or speaking), blurred vision or diplopia, symmetric descending weakness in a proximal to distal pattern, and respiratory dysfunction from respiratory muscle paralysis or upper airway obstruction without sensory deficits. Inhalational botulism would have a similar clinical presentation as food-borne botulism however, the gastrointestinal symptoms that accompany foodborne botulism may be absent. 

The presence of cranial neuropathy may result in a misdiagnosis of brainstem stroke. Cranial nerve palsies may result from local pressure from the false internal carotid artery lumen, thromboembolism or hemodynamic compromise to the blood supply of the nerve. Cranial nerve III receives its blood supply from the ophthalmic artery, branches of the internal carotid or the posterior cerebral artery and, consequently, may rarely become ischemic after carotid dissection. 

Studies on monkeys have demonstrated visual loss and optic atrophy with intravitreous injection of vincristine. Clinical reports of postvincristine optic atrophy are rare. Most are irreversible, progressing to permanent blindness. There is commonly coexistent peripheral or cranial neuropathy (65). It is possible that certain patients are predisposed to vincristine-induced optic atrophy. Optic neuropathy after a single small dose of vincristine has been reported in a single case the dose of vincristine was small (1275 mg), and the latent period before onset of visual loss was brief (6-8 weeks) (66). Previously reported cases have had multiple injections of vincristine and the latent period was longer than 3 months. 

Symmetrical cranial neuropathies, such as ptosis, weakened jaw clench, dysarthria, dysphonia and dysphagia, and often enlarged or sluggishly reactive pupils... 

The eyelid disorders may be related not only to neuromuscular transmission, as in myasthenia gravis, but also to intrinsic muscle weakness and cranial neuropathy. 

Jabs DA, Houk JL, Bias WB, et al. Familial granulomatous synovitis, uveitis, and cranial neuropathies. Am J Med 1985 78(5) 801-804. 

The clinical presentation of MM in HIV-infected patients is similar to that in other patients with vasculitic neuropathy (Hoke and Comblath 2004). It is characterized by symptoms and signs of sensory involvement, with numbness and tingling in the distribution of one peripheral nerve trunk. Sequential involvement of other noncontiguous peripheral or cranial nerves progresses over days to weeks. The initial multifocal and random neurologic features may evolve to symmetrical neuropathy (Ferrari et al. 2006). 

Acute exposure to trichloroethylene and its decomposition products (e.g., dichloroacetylene) has also led to residual neuropathy, characterized by nerve damage. This neuropathy is characterized by facial numbness, jaw weakness, and facial discomfort (indicating damage to cranial nerves V and VII) which can persist for several months (Buxton and Hayward 1967 Feldman 1970). Chronic exposure in the workplace has also been associated with damage to the cranial nerves in several cases (Bardodej and Vyskocil 1956 Barret et al. 1987 Cavanagh and Buxton 1989). Persons who have died from overexposure have shown degeneration of cranial nuclei in the brain stem (Buxton and Hayward 1967). Some of these effects may be attributed to... 

It is not clear if the effects on cranial nerve dysfunction from inhalation exposure are attributable to trichloroethylene or its decomposition products. For example, while a number of limited animal studies report neuropathies associated with exposure to trichloroethylene (Bardodej and Vyskocil 1956 Barret et al. 1987 Lawrence and Partyka 1981 McCunney 1988), there are some animal studies which report that these effects resulted from exposure to the trichloroethylene decomposition product, dichloroacetylene (Barret et al. 1992 Buxton and Hayward 1967 Cavanagh and Buxton 1989 Feldman 1970 Humphrey and McClelland 1944). 

Peripheral neuropathy primary dose-limiting toxicity motor sensory, autonomic, and cranial nerves may all be affected (paresthesias, ileus, urinary retention, facial palsies) may be irreversible mild emetogen SIADH vesicant extravasation injury... 

Diabetes mellitus is the most common cause of peripheral neuropathy in the United States. Approximately half of all diabetics demonstrate evidences of neuropathy. The usual clinical pattern is that of a slowly progressive, mixed sensorimotor and autonomic polyneuropathy. More acute, asymmetrical motor neuropathies are also seen, usually affecting the lumbosacral plexus, particularly in older persons with type 2 (non-insulin-dependent) diabetes mellitus. Patients with diabetes mellitus are also prone to develop isolated palsies of cranial nerve III or VII, and there is a high incidence of asymptomatic focal demyelin-ation in the distal median nerve. 

The main dose-limiting toxicity is neurotoxicity, usually expressed as a peripheral sensory neuropathy, although autonomic nervous system dysfunction with orthostatic hypotension, urinary retention, paralytic ileus, or constipation, cranial nerve palsies, ataxia, seizures, and coma have been observed. While myelosuppression occurs, it is generally milder and much less significant than with vinblastine. The other potential adverse effect that can develop is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). 

Central and/or peripheral nervous system involvement is one of the most frequent features, often resulting in the neonatal period in drowsiness, poor sucking, severe hypotonia, abnormal movements, seizures, respiratory distress, and fatal keto-acidotic coma with lactic acidosis [3]. To these severe conditions echo late-onset diseases now frequently attributed to or associated with mitochondrial OXPHOS defects, such as Alzheimer s or Parkinsons disease [10]. Major neurological symptoms, in variable combinations, involve trunk hypotonia, cranial nerve and brainstem involvement (with abnormal eye movements, ophthalmoplegia, recurrent apneas), cerebellar ataxia, myoclonia, seizures, pyramidal syndrome, peripheral neuropathy, poliodystrophy, and leukodystrophy infections [27,28]. A diffuse impairment of the cerebral white matter (leukodystrophy) mostly results in motor disturbance with mental retardation and low incidence of seizures. 

One type of familial amyloidosis first identified in the Finnish population is caused by deposition of gelsolin (Maury et al., 2000 Maury et al., 2001). This Finnish type familial amyloidosis (FAF) is a hereditable autosomal dominant amyloid polyneuropathy, characterized by corneal lattice dystrophy, progressive cranial and peripheral neuropathy as well as skin changes (Chen et al., 2001 Maury et al., 2001). 

A review of certain chemicals is essential. Ethylene glycol is an antifreeze used for gasoline engines and may produce somnolence, imreactive pupils, disc swelling, and kidney failure. Systemic lead poisoning produces headaches, coma, cranial nerve palsies, and papilledema. Wood alcohol, or methanol, may produce severe toxic neuropathy and disc edema. Drugs known to produce toxic optic neuropathy include amiodarone (an antiar-rhythmic), quinine, aminoquinolines, ibuprofen, ethambutol, isoniazid, and chloramphenicol. 

Encephalopathy, peripheral neuropathy, cerebellar syndromes, autonomic neuropathy, and cranial nerve toxicity represent the range of neurological complications associated with cancer chemotherapy. Dose, route of administration, age of the patient, hepatic and renal function, prior and/or concomitant use of other neurotoxic drugs, and the concurrent use of cranial or CNS radiotherapy can each influence the incidence rate and severity of neurologic symptoms associated with selected chemotherapy drugs. 

In addition to a normal eye, vision requires an intact circuit to and from the brain itself. The optic nerve (cranial nerve II), for example, carries retinal information to the occipital cortex in the posterior aspects of the brain. In addition, information concerning pupil size, direction of gaze, simultaneous movement of the eyes (conjugate gaze), and focus clarity is relayed from the brain back to the eye through multiple nerves. Ethambutol, an antituberculous medication, affects the optic nerves (optic neuropathy) whereas organic mercury compounds have been historically associated with toxic effects on the occipital cortex (cortical blindness). 

Absence of bulbar palsies positive rapid antigen test result or throat culture Normal EMG in conversion paralysis Absence of bulbar palsies and flaccid paralysis Elevated creatine kinase levels Sensory neuropathy few cranial nerve palsies Absence of bulbar palsies and acute flaccid paralysis... 

---